Objective: Alzheimer's disease is one of the most common neurodegenerative diseases, and mechanisms of its development have been studied for many years. The aim of the research was to study the content of thyroid-stimulating hormone (TSH), thyroid hormones and tau protein in the blood serum, as well as the content of thyroid hormones and some neurotransmitters in the cerebral cortex in the dynamics of experimental Alzheimer’s disease in rats.

Materials and methods. The experiment was performed on 45 WAG rats, which were divided into 3 groups. The first group was the control one. Animals from the second and third groups were intraperitoneally administered with scopolamine for 14 and 27 days, which led to the development of Alzheimer's disease. Brain homogenate was prepared. Concentrations of T3, T4 in blood serum and homogenates of the cerebral cortex, as well as TSH and tau protein in serum, were determined by ELISA. Determination of the content of neurotransmitter amino acids (aspartate and glutamate) was carried out by thin-layer chromatography. The content of dopamine and norepinephrine in the cerebral cortex homogenate was determined by column chromatography, and acetylcholine levels were measured by spectrophotometry. Morphological examination included staining of brain tissue with congo-rot + hematoxylin.

Results. It was established that in cerebral cortex homogenates of rats with experimental Alzheimer’s disease the T3 content was reduced, and T4 levels were similar to rats of the control group, which in combination with the normal concentration of thyroid hormones in blood serum indicates the development of local hypothyroidism in the cerebral cortex. In rats with Alzheimer's disease, glutamic and aspartic acid levels were increased against the background of GABA reduction. There was also a decrease in the levels of noradrenaline and dopamine in the cerebral cortex homogenates, which contributes to the abnormal energy metabolism and impaired cognitive functions. Morphological study demonstrated the presence of congophilic masses in the brain tissue and in the walls of small arteries with the development of brain atrophy.

Conclusions. Alzheimer's disease caused by the administration of scopalamine is characterized by the development of local hypothyroidism in the cerebral cortex, an increase in the level of glutamic and aspartic acids with a decrease in GABA, a decrease in the level of dopamine and norepinephrine in the cerebral cortex.

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